Patterns of interstitial inflammation during the evolution of renal injury in experimental aristolochic acid nephropathy
Background. Interstitial inflammation is a prominent feature associated with the severity of renal injury and progressive kidney failure. We utilized an animal model of aristolochic acid (AA)-induced nephropathy (AAN) to assess patterns of infiltration and inflammation during the evolution of tubulo...
Gespeichert in:
| Veröffentlicht in: | Nephrology, dialysis, transplantation dialysis, transplantation, 2008-08, Vol.23 (8), p.2480-2491 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2491 |
|---|---|
| container_issue | 8 |
| container_start_page | 2480 |
| container_title | Nephrology, dialysis, transplantation |
| container_volume | 23 |
| creator | Pozdzik, Agnieszka A. Salmon, Isabelle J. Husson, Cécile P. Decaestecker, Christine Rogier, Edith Bourgeade, Marie-Françoise Deschodt-Lanckman, Monique M. Vanherweghem, Jean-Louis Nortier, Joëlle L. |
| description | Background. Interstitial inflammation is a prominent feature associated with the severity of renal injury and progressive kidney failure. We utilized an animal model of aristolochic acid (AA)-induced nephropathy (AAN) to assess patterns of infiltration and inflammation during the evolution of tubulointerstitial damage and to relate them to the development of fibrosis. Methods. Male Wistar rats receiving sc daily AA or vehicle were sacrificed between Days 1 and 35. Infiltrating mononuclear cells were characterized by immunohistochemistry. The kidney infiltrating T lymphocytes were phenotyped by flow cytometry. Urinary levels of Th-1/ Th-2 cytokines, of monocyte chemoattractant protein-1 and of active transforming growth factor-beta (TGF-β) were measured. Tissue expression of phosphorylated smad 2/3 protein was used to examine the TGF-β signalling pathway. Results. In AA rats, monocytes/macrophages and T lymphocytes predominantly infiltrated areas of necrotic proximal tubular cells. The coexpressions of ED1 and/or Ki-67/MHCII by infiltrating cells reflected monocyte/macrophage proliferation and their activation, respectively. The accumulation of cytotoxic T lymphocytes was attested by severe signs of CD8+ cell tubulitis. The CD8/E-cadherin costaining confirmed intrarenal homing of CD8+CD103+ cells. Urinary levels of proinflammatory cytokines and of active TGF-β significantly increased at Days 10 and 35. An early and persistent nuclear overexpression of phosphorylated smad 2/3 protein was detected in tubular and interstitial compartments. Conclusion. An early and massive interstitial inflammation characterized by activated monocytes/macrophages and cytotoxic CD8+CD103+ T lymphocytes is demonstrated for the first time during the progression of experimental AAN. The involvement in an interstitial fibrosis onset of active TGF-β is highly suggested, at least via the psmad2/3 intracellular signalling pathway. |
| doi_str_mv | 10.1093/ndt/gfn140 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_218165385</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/ndt/gfn140</oup_id><sourcerecordid>1522667721</sourcerecordid><originalsourceid>FETCH-LOGICAL-c410t-487324873da771b45becd379768c0483164df2605c22c84e6dc81b28abc4ef863</originalsourceid><addsrcrecordid>eNp9kFtPwyAUgInR6Ly8-ANMY-KLSRUoLezRLLqZLHEaTYwvhFLqmB1UoGb797JL5puEcODwcYAPgHMEbxDsZ7emCreftUEE7oEeIgVMccbyfdCLmyiFOewfgWPvZxDCPqb0EBwhFoHYe2AxESEoZ3xi60SbOPVBBy2auKgbMZ-LoK1Jqs5p85mEqUrUj226dTKecMqs0VnnljEkatEqp-fKhJgWTvtgGyunWiZC6ioxqp0624owXZ6Cg1o0Xp1t4wl4e7h_HYzS8dPwcXA3TiVBMKSE0QyvhkpQikqSl0pWGe3TgklIWIYKUtW4gLnEWDKiikoyVGImSklUzYrsBFxu6rbOfnfKBz6znYuv9hwjhoqVhghdbyDprPdO1byNvxBuyRHkK8c8OuYbxxG-2Fbsyrmq_tCt1AhcbQHhpWhqJ4zUfsdhmNPYyB9nu_b_C9MNF3WqxY4U7osXNKM5H71_8JfhcPKcD0f8I_sFAEejfw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>218165385</pqid></control><display><type>article</type><title>Patterns of interstitial inflammation during the evolution of renal injury in experimental aristolochic acid nephropathy</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Pozdzik, Agnieszka A. ; Salmon, Isabelle J. ; Husson, Cécile P. ; Decaestecker, Christine ; Rogier, Edith ; Bourgeade, Marie-Françoise ; Deschodt-Lanckman, Monique M. ; Vanherweghem, Jean-Louis ; Nortier, Joëlle L.</creator><creatorcontrib>Pozdzik, Agnieszka A. ; Salmon, Isabelle J. ; Husson, Cécile P. ; Decaestecker, Christine ; Rogier, Edith ; Bourgeade, Marie-Françoise ; Deschodt-Lanckman, Monique M. ; Vanherweghem, Jean-Louis ; Nortier, Joëlle L.</creatorcontrib><description>Background. Interstitial inflammation is a prominent feature associated with the severity of renal injury and progressive kidney failure. We utilized an animal model of aristolochic acid (AA)-induced nephropathy (AAN) to assess patterns of infiltration and inflammation during the evolution of tubulointerstitial damage and to relate them to the development of fibrosis. Methods. Male Wistar rats receiving sc daily AA or vehicle were sacrificed between Days 1 and 35. Infiltrating mononuclear cells were characterized by immunohistochemistry. The kidney infiltrating T lymphocytes were phenotyped by flow cytometry. Urinary levels of Th-1/ Th-2 cytokines, of monocyte chemoattractant protein-1 and of active transforming growth factor-beta (TGF-β) were measured. Tissue expression of phosphorylated smad 2/3 protein was used to examine the TGF-β signalling pathway. Results. In AA rats, monocytes/macrophages and T lymphocytes predominantly infiltrated areas of necrotic proximal tubular cells. The coexpressions of ED1 and/or Ki-67/MHCII by infiltrating cells reflected monocyte/macrophage proliferation and their activation, respectively. The accumulation of cytotoxic T lymphocytes was attested by severe signs of CD8+ cell tubulitis. The CD8/E-cadherin costaining confirmed intrarenal homing of CD8+CD103+ cells. Urinary levels of proinflammatory cytokines and of active TGF-β significantly increased at Days 10 and 35. An early and persistent nuclear overexpression of phosphorylated smad 2/3 protein was detected in tubular and interstitial compartments. Conclusion. An early and massive interstitial inflammation characterized by activated monocytes/macrophages and cytotoxic CD8+CD103+ T lymphocytes is demonstrated for the first time during the progression of experimental AAN. The involvement in an interstitial fibrosis onset of active TGF-β is highly suggested, at least via the psmad2/3 intracellular signalling pathway.</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfn140</identifier><identifier>PMID: 18385385</identifier><identifier>CODEN: NDTREA</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; aristolochic acid ; Aristolochic Acids - toxicity ; Biological and medical sciences ; Disease Models, Animal ; Emergency and intensive care: renal failure. Dialysis management ; Fibrosis ; Intensive care medicine ; Kidney - drug effects ; Kidney - pathology ; Kidney - physiopathology ; Kidney Failure, Chronic - chemically induced ; Kidney Failure, Chronic - pathology ; Kidney Failure, Chronic - physiopathology ; macrophages ; Macrophages - immunology ; Macrophages - pathology ; Male ; Medical sciences ; Monocytes - immunology ; Monocytes - pathology ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Rats ; Rats, Wistar ; Renal failure ; renal fibrosis ; Signal Transduction ; Smad2 Protein - metabolism ; Smad3 Protein - metabolism ; T lymphocytes ; T-Lymphocytes - immunology ; T-Lymphocytes - pathology ; Transforming Growth Factor beta - metabolism ; transforming growth factor-β</subject><ispartof>Nephrology, dialysis, transplantation, 2008-08, Vol.23 (8), p.2480-2491</ispartof><rights>Oxford University Press © The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org 2008</rights><rights>2008 INIST-CNRS</rights><rights>The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c410t-487324873da771b45becd379768c0483164df2605c22c84e6dc81b28abc4ef863</citedby><cites>FETCH-LOGICAL-c410t-487324873da771b45becd379768c0483164df2605c22c84e6dc81b28abc4ef863</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1578,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20577774$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18385385$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pozdzik, Agnieszka A.</creatorcontrib><creatorcontrib>Salmon, Isabelle J.</creatorcontrib><creatorcontrib>Husson, Cécile P.</creatorcontrib><creatorcontrib>Decaestecker, Christine</creatorcontrib><creatorcontrib>Rogier, Edith</creatorcontrib><creatorcontrib>Bourgeade, Marie-Françoise</creatorcontrib><creatorcontrib>Deschodt-Lanckman, Monique M.</creatorcontrib><creatorcontrib>Vanherweghem, Jean-Louis</creatorcontrib><creatorcontrib>Nortier, Joëlle L.</creatorcontrib><title>Patterns of interstitial inflammation during the evolution of renal injury in experimental aristolochic acid nephropathy</title><title>Nephrology, dialysis, transplantation</title><addtitle>Nephrol Dial Transplant</addtitle><addtitle>Nephrol Dial Transplant</addtitle><description>Background. Interstitial inflammation is a prominent feature associated with the severity of renal injury and progressive kidney failure. We utilized an animal model of aristolochic acid (AA)-induced nephropathy (AAN) to assess patterns of infiltration and inflammation during the evolution of tubulointerstitial damage and to relate them to the development of fibrosis. Methods. Male Wistar rats receiving sc daily AA or vehicle were sacrificed between Days 1 and 35. Infiltrating mononuclear cells were characterized by immunohistochemistry. The kidney infiltrating T lymphocytes were phenotyped by flow cytometry. Urinary levels of Th-1/ Th-2 cytokines, of monocyte chemoattractant protein-1 and of active transforming growth factor-beta (TGF-β) were measured. Tissue expression of phosphorylated smad 2/3 protein was used to examine the TGF-β signalling pathway. Results. In AA rats, monocytes/macrophages and T lymphocytes predominantly infiltrated areas of necrotic proximal tubular cells. The coexpressions of ED1 and/or Ki-67/MHCII by infiltrating cells reflected monocyte/macrophage proliferation and their activation, respectively. The accumulation of cytotoxic T lymphocytes was attested by severe signs of CD8+ cell tubulitis. The CD8/E-cadherin costaining confirmed intrarenal homing of CD8+CD103+ cells. Urinary levels of proinflammatory cytokines and of active TGF-β significantly increased at Days 10 and 35. An early and persistent nuclear overexpression of phosphorylated smad 2/3 protein was detected in tubular and interstitial compartments. Conclusion. An early and massive interstitial inflammation characterized by activated monocytes/macrophages and cytotoxic CD8+CD103+ T lymphocytes is demonstrated for the first time during the progression of experimental AAN. The involvement in an interstitial fibrosis onset of active TGF-β is highly suggested, at least via the psmad2/3 intracellular signalling pathway.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>aristolochic acid</subject><subject>Aristolochic Acids - toxicity</subject><subject>Biological and medical sciences</subject><subject>Disease Models, Animal</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Fibrosis</subject><subject>Intensive care medicine</subject><subject>Kidney - drug effects</subject><subject>Kidney - pathology</subject><subject>Kidney - physiopathology</subject><subject>Kidney Failure, Chronic - chemically induced</subject><subject>Kidney Failure, Chronic - pathology</subject><subject>Kidney Failure, Chronic - physiopathology</subject><subject>macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Monocytes - immunology</subject><subject>Monocytes - pathology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Renal failure</subject><subject>renal fibrosis</subject><subject>Signal Transduction</subject><subject>Smad2 Protein - metabolism</subject><subject>Smad3 Protein - metabolism</subject><subject>T lymphocytes</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - pathology</subject><subject>Transforming Growth Factor beta - metabolism</subject><subject>transforming growth factor-β</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kFtPwyAUgInR6Ly8-ANMY-KLSRUoLezRLLqZLHEaTYwvhFLqmB1UoGb797JL5puEcODwcYAPgHMEbxDsZ7emCreftUEE7oEeIgVMccbyfdCLmyiFOewfgWPvZxDCPqb0EBwhFoHYe2AxESEoZ3xi60SbOPVBBy2auKgbMZ-LoK1Jqs5p85mEqUrUj226dTKecMqs0VnnljEkatEqp-fKhJgWTvtgGyunWiZC6ioxqp0624owXZ6Cg1o0Xp1t4wl4e7h_HYzS8dPwcXA3TiVBMKSE0QyvhkpQikqSl0pWGe3TgklIWIYKUtW4gLnEWDKiikoyVGImSklUzYrsBFxu6rbOfnfKBz6znYuv9hwjhoqVhghdbyDprPdO1byNvxBuyRHkK8c8OuYbxxG-2Fbsyrmq_tCt1AhcbQHhpWhqJ4zUfsdhmNPYyB9nu_b_C9MNF3WqxY4U7osXNKM5H71_8JfhcPKcD0f8I_sFAEejfw</recordid><startdate>20080801</startdate><enddate>20080801</enddate><creator>Pozdzik, Agnieszka A.</creator><creator>Salmon, Isabelle J.</creator><creator>Husson, Cécile P.</creator><creator>Decaestecker, Christine</creator><creator>Rogier, Edith</creator><creator>Bourgeade, Marie-Françoise</creator><creator>Deschodt-Lanckman, Monique M.</creator><creator>Vanherweghem, Jean-Louis</creator><creator>Nortier, Joëlle L.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope></search><sort><creationdate>20080801</creationdate><title>Patterns of interstitial inflammation during the evolution of renal injury in experimental aristolochic acid nephropathy</title><author>Pozdzik, Agnieszka A. ; Salmon, Isabelle J. ; Husson, Cécile P. ; Decaestecker, Christine ; Rogier, Edith ; Bourgeade, Marie-Françoise ; Deschodt-Lanckman, Monique M. ; Vanherweghem, Jean-Louis ; Nortier, Joëlle L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c410t-487324873da771b45becd379768c0483164df2605c22c84e6dc81b28abc4ef863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>aristolochic acid</topic><topic>Aristolochic Acids - toxicity</topic><topic>Biological and medical sciences</topic><topic>Disease Models, Animal</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Fibrosis</topic><topic>Intensive care medicine</topic><topic>Kidney - drug effects</topic><topic>Kidney - pathology</topic><topic>Kidney - physiopathology</topic><topic>Kidney Failure, Chronic - chemically induced</topic><topic>Kidney Failure, Chronic - pathology</topic><topic>Kidney Failure, Chronic - physiopathology</topic><topic>macrophages</topic><topic>Macrophages - immunology</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Monocytes - immunology</topic><topic>Monocytes - pathology</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Renal failure</topic><topic>renal fibrosis</topic><topic>Signal Transduction</topic><topic>Smad2 Protein - metabolism</topic><topic>Smad3 Protein - metabolism</topic><topic>T lymphocytes</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - pathology</topic><topic>Transforming Growth Factor beta - metabolism</topic><topic>transforming growth factor-β</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pozdzik, Agnieszka A.</creatorcontrib><creatorcontrib>Salmon, Isabelle J.</creatorcontrib><creatorcontrib>Husson, Cécile P.</creatorcontrib><creatorcontrib>Decaestecker, Christine</creatorcontrib><creatorcontrib>Rogier, Edith</creatorcontrib><creatorcontrib>Bourgeade, Marie-Françoise</creatorcontrib><creatorcontrib>Deschodt-Lanckman, Monique M.</creatorcontrib><creatorcontrib>Vanherweghem, Jean-Louis</creatorcontrib><creatorcontrib>Nortier, Joëlle L.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pozdzik, Agnieszka A.</au><au>Salmon, Isabelle J.</au><au>Husson, Cécile P.</au><au>Decaestecker, Christine</au><au>Rogier, Edith</au><au>Bourgeade, Marie-Françoise</au><au>Deschodt-Lanckman, Monique M.</au><au>Vanherweghem, Jean-Louis</au><au>Nortier, Joëlle L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Patterns of interstitial inflammation during the evolution of renal injury in experimental aristolochic acid nephropathy</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><stitle>Nephrol Dial Transplant</stitle><addtitle>Nephrol Dial Transplant</addtitle><date>2008-08-01</date><risdate>2008</risdate><volume>23</volume><issue>8</issue><spage>2480</spage><epage>2491</epage><pages>2480-2491</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><coden>NDTREA</coden><abstract>Background. Interstitial inflammation is a prominent feature associated with the severity of renal injury and progressive kidney failure. We utilized an animal model of aristolochic acid (AA)-induced nephropathy (AAN) to assess patterns of infiltration and inflammation during the evolution of tubulointerstitial damage and to relate them to the development of fibrosis. Methods. Male Wistar rats receiving sc daily AA or vehicle were sacrificed between Days 1 and 35. Infiltrating mononuclear cells were characterized by immunohistochemistry. The kidney infiltrating T lymphocytes were phenotyped by flow cytometry. Urinary levels of Th-1/ Th-2 cytokines, of monocyte chemoattractant protein-1 and of active transforming growth factor-beta (TGF-β) were measured. Tissue expression of phosphorylated smad 2/3 protein was used to examine the TGF-β signalling pathway. Results. In AA rats, monocytes/macrophages and T lymphocytes predominantly infiltrated areas of necrotic proximal tubular cells. The coexpressions of ED1 and/or Ki-67/MHCII by infiltrating cells reflected monocyte/macrophage proliferation and their activation, respectively. The accumulation of cytotoxic T lymphocytes was attested by severe signs of CD8+ cell tubulitis. The CD8/E-cadherin costaining confirmed intrarenal homing of CD8+CD103+ cells. Urinary levels of proinflammatory cytokines and of active TGF-β significantly increased at Days 10 and 35. An early and persistent nuclear overexpression of phosphorylated smad 2/3 protein was detected in tubular and interstitial compartments. Conclusion. An early and massive interstitial inflammation characterized by activated monocytes/macrophages and cytotoxic CD8+CD103+ T lymphocytes is demonstrated for the first time during the progression of experimental AAN. The involvement in an interstitial fibrosis onset of active TGF-β is highly suggested, at least via the psmad2/3 intracellular signalling pathway.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>18385385</pmid><doi>10.1093/ndt/gfn140</doi><tpages>12</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0931-0509 |
| ispartof | Nephrology, dialysis, transplantation, 2008-08, Vol.23 (8), p.2480-2491 |
| issn | 0931-0509 1460-2385 |
| language | eng |
| recordid | cdi_proquest_journals_218165385 |
| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals aristolochic acid Aristolochic Acids - toxicity Biological and medical sciences Disease Models, Animal Emergency and intensive care: renal failure. Dialysis management Fibrosis Intensive care medicine Kidney - drug effects Kidney - pathology Kidney - physiopathology Kidney Failure, Chronic - chemically induced Kidney Failure, Chronic - pathology Kidney Failure, Chronic - physiopathology macrophages Macrophages - immunology Macrophages - pathology Male Medical sciences Monocytes - immunology Monocytes - pathology Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Rats Rats, Wistar Renal failure renal fibrosis Signal Transduction Smad2 Protein - metabolism Smad3 Protein - metabolism T lymphocytes T-Lymphocytes - immunology T-Lymphocytes - pathology Transforming Growth Factor beta - metabolism transforming growth factor-β |
| title | Patterns of interstitial inflammation during the evolution of renal injury in experimental aristolochic acid nephropathy |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-02T19%3A34%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Patterns%20of%20interstitial%20inflammation%20during%20the%20evolution%20of%20renal%20injury%20in%20experimental%20aristolochic%20acid%20nephropathy&rft.jtitle=Nephrology,%20dialysis,%20transplantation&rft.au=Pozdzik,%20Agnieszka%20A.&rft.date=2008-08-01&rft.volume=23&rft.issue=8&rft.spage=2480&rft.epage=2491&rft.pages=2480-2491&rft.issn=0931-0509&rft.eissn=1460-2385&rft.coden=NDTREA&rft_id=info:doi/10.1093/ndt/gfn140&rft_dat=%3Cproquest_cross%3E1522667721%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=218165385&rft_id=info:pmid/18385385&rft_oup_id=10.1093/ndt/gfn140&rfr_iscdi=true |